318 lines
33 KiB
Markdown
318 lines
33 KiB
Markdown
---
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title: "Ventriculomegaly"
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docid: "f40bd6eb-e7e5-498a-8bde-ad6bcd546f21"
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authors:
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- key: "47381de4-c9fd-4999-8dd0-1808cd72db6b"
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value: "Luke L. Linscott, MD"
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breadcrumbs:
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-
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name: "Brain"
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slug: "brain"
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treeNodeId: "6d8829f1-14d7-45af-8675-255189aa526a"
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-
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name: "Differential Diagnosis"
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slug: "differential-diagnosis"
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treeNodeId: "a7fdd139-664e-4bb8-8d18-400e4733ff60"
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-
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name: "Ventricles, Periventricular Regions"
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slug: "ventricles-periventricular-regions"
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treeNodeId: "353c434a-a6fc-4ef1-8786-d30a1988a4dc"
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-
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name: "Generic Imaging Patterns"
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slug: "generic-imaging-patterns"
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treeNodeId: "969c31a2-ef56-4fc3-9125-05857cf9aac3"
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-
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name: "Ventriculomegaly"
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slug: "ventriculomegaly"
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treeNodeId: null
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category: "Brain"
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documentVersionId: "69dd2446-06ad-4f37-bba3-f59d4c5d40b8"
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imageCount: 26
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lastUpdated: "01/23/23"
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pageDescription: "Ventriculomegaly"
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pageKeywords: "Brain, Differential Diagnosis, Ventricles, Periventricular Regions, Generic Imaging Patterns, Ventriculomegaly"
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pageTitle: "Ventriculomegaly | STATdx"
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enhancedTitle: "Ventriculomegaly"
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type: "DDX"
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references: true
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breadcrumbs:
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- "Brain"
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- "Differential Diagnosis"
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- "Ventricles, Periventricular Regions"
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- "Generic Imaging Patterns"
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- "Ventriculomegaly"
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---
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# ESSENTIAL INFORMATION
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- ## Key Differential Diagnosis Issues
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- 2 main causes of ventriculomegaly
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- ↑ CSF pressures → hydrocephalus
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- ↓ brain volume → passive ventricular enlargement
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- Clinical features to consider
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- Head circumference is critical to interpreting significance of enlarged ventricles
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- ↑ head size: Hydrocephalus
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- ↓ head size: Brain parenchymal volume loss
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- Patients may come to clinical attention during prenatal screening or well-child check-ups
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- Imaging features of hydrocephalus
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- Etiologies to consider
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- Obstruction usually occurs at cerebral aqueduct, foramen of Monro, or 4th ventricular outlets
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- e.g., aqueductal stenosis, obstructing tumor
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- Communicating hydrocephalus is due to CSF overproduction or poor CSF resorption
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- e.g., choroid plexus papilloma, benign enlargement of subarachnoid spaces
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- Some etiologies can cause either or mixed forms
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- e.g., posthemorrhagic, postinfectious, vein of Galen malformation (VGAM)
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- Imaging signs of hydrocephalus
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- Macrocephaly: ↑ craniofacial ratio
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- Rounded margins of lateral ventricles, depressed floor of 3rd ventricle
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- Transependymal edema: Periventricular white matter (WM) ↑ T2/FLAIR signal, greatest at frontal & occipital horns; effacement of cerebral sulci & basilar cisterns
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- Imaging features of volume loss
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- Etiologies to consider
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- Diffuse vs. focal cortical ischemia
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- e.g., hypoxic-ischemic encephalopathy (HIE) vs. arterial ischemic stroke
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- Symmetric vs. focal WM volume loss
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- e.g., periventricular leukomalacia vs. porencephaly
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- Imaging signs of brain parenchymal volume loss
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- Microcephaly: ↓ craniofacial ratio
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- Angular margins of lateral ventricles
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- Prominent sulci & basilar cisterns
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- Modality considerations
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- Fetal US for detection of in utero ventriculomegaly
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- Fetal MR is excellent for underlying/associated anomalies
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- US is important tool for initial evaluation of neonates/infants with suspected ventriculomegaly
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- Requires open anterior fontanelle
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- CT is often 1st-line modality in acute presentations
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- MR is most definitive test for determination of underlying cause of ventriculomegaly
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- Best test for determining cause of hydrocephalus
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- Best evaluation of brain parenchyma to detect possible volume loss
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- ## Helpful Clues for Common Diagnoses
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- **Fetal Ventriculomegaly**
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- Likelihood of normal neurologic development based on lateral ventricular size in utero
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- Mild (10-12 mm): > 90%
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- Moderate (13-15 mm): 80-93%
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- Severe (> 15 mm): ~ 62%
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- Underlying causes of fetal ventriculomegaly
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- Infectious (e.g., CMV), genetic (e.g., trisomy), malformations (e.g., Chiari 2)
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- CMV testing & amniocentesis typically performed
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- Obstructive causes considered separately
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- **Benign Enlargement of Subarachnoid Spaces**
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- a.k.a. benign hydrocephalus of infancy, benign macrocrania of infancy, external hydrocephalus
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- Enlarged subarachnoid spaces (SAS) ± mild ventriculomegaly
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- Findings develop in 1st few months of life & usually resolve by ~ 2 years of age
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- Often family history of macrocephaly
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- Normal development or mild developmental delay
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- Imaging: Prominent SAS over frontal & parietal convexities with normal vessels traversing SAS
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- No displacement of arachnoid membrane from dura (i.e., no subdural fluid)
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- **Chiari 2 Malformation**
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- Brain malformation due to open neural tube defect (most commonly lumbosacral myelomeningocele)
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- Hydrocephalus requiring shunting occurs almost universally without in utero surgical repair
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- Imaging: Small posterior fossa, inferior migration of cerebellum/brainstem, beaked tectum, dysplastic corpus callosum, scalloping of dorsal clivus
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- **Aqueductal Stenosis**
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- Congenital atresia/stenosis of cerebral aqueduct
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- Imaging: Lateral & 3rd ventricle dilation with normal 4th ventricle
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- Narrowed/absent cerebral aqueduct on 3D SSFP MR
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- Lack of flow void within cerebral aqueduct on T2
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- **Acquired Hydrocephalus**
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- 2 main types: Communicating & noncommunicating
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- Communicating: ↑ production or ↓ resorption of CSF
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- Obstructive: Blockage of ventricular outlets
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- Depending on cause, may present enlarging head or signs of ↑ intracranial pressure
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- May have signs of ↑ intracranial pressure
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- Treatment: Shunting or 3rd ventriculostomy
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- **Posthemorrhagic hydrocephalus**
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- Most common in premature infants with germinal matrix/intraventricular hemorrhage (IVH)
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- Look for hemosiderin along ventricles/brainstem
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- SWI/GRE is most sensitive for detection of prior IVH
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- **Acute infectious hydrocephalus**
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- During acute bacterial infection, ↑ head size may occur due to ↑ extraaxial spaces from meningitis & subdural/epidural empyema
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- **Postinfectious hydrocephalus**
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- Obstruction may occur due to synechiae
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- Communicating hydrocephalus may occur due to arachnoid granulation dysfunction
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- **Obstructing tumor**
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- Smaller tumors in critical locations may obstruct
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- e.g., subependymal giant cell astrocytoma (SEGA) at foramen of Monro, tectal plate glioma at cerebral aqueduct
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- Larger tumors anywhere in brain may obstruct, particularly in posterior fossa
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- **CSF overproduction (choroid plexus tumors)**
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- Choroid plexus papilloma/carcinoma causes CSF overproduction
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- Inability to resorb excess CSF → ↑ ventricular size
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- **Brain Volume Loss**
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- Results in ventricular enlargement
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- Focal (e.g., porencephaly, stroke)
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- Symmetric (e.g., periventricular leukomalacia, metabolic disease)
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- **Hypoxic-ischemic injury**
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- Often results in symmetric or asymmetric brain volume loss & associated ventricular enlargement
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- Look for characteristic patterns of injury (e.g., perirolandic or watershed)
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- **Arterial ischemic stroke**
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- Most often occurs in perinatal period or related to embolic phenomenon
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- Encephalomalacia develops in arterial territory with focal ventricular enlargement
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- **Periventricular leukomalacia**
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- Sequelae of WM injury of prematurity
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- Usually symmetric WM volume loss with little or no associated gliosis (↑ FLAIR signal)
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- **Porencephaly**
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- Most often results from grade 4 IVH, but any insult early in development may cause porencephaly
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- Porencephaly develops rather than encephalomalacia as no astrocytic response occurs in very young brains
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- **Metabolic brain disease**
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- Numerous diseases cause significant brain volume loss, resulting in ventriculomegaly
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- Usually symmetric; may be
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- Frontal predominant (e.g., Alexander disease)
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- Posterior predominant (e.g., X-linked adrenoleukodystrophy)
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- Diffuse (e.g., metachromatic leukodystrophy)
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- ## Helpful Clues for Less Common Diagnoses
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- **Hemimegalencephaly**
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- Unilateral abnormal neuronal proliferation & migration
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- Neonate/infant: ↑ T1 & ↓ T2 in WM with blurred gray matter/WM junctions
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- Often shows enlarged ipsilateral ventricle
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- **Vein of Galen Aneurysmal Malformation**
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- Ectatic vascular structure is median prosencephalic vein, not vein of Galen, which never forms
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- High-flow vascular malformation due to direct communication between arteries & median prosencephalic vein
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- Ventricular enlargement may occur due to
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- Mass effect of malformation on cerebral aqueduct
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- ↑ venous pressure & poor CSF resorption
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- Parenchymal insult with volume loss
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- After birth, ↑ in blood flow through malformation
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- Up to 80% of left ventricular output may supply brain
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- Leads to ↑ cardiac output & heart failure
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- **Dandy-Walker Malformation**
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- Vermian hypoplasia with large posterior fossa cyst that communicates with 4th ventricle but not SAS
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- Lambdoid-torcular inversion
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- Often associated with hydrocephalus
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- **Hydranencephaly**
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- In utero destruction of brain in internal carotid artery territories
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- May cause poor CSF regulation & hydrocephalus, requiring shunting
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- **Holoprosencephaly**
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- Holoprosencephaly (alobar form) often develops ↑ size of monoventricle over time
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- Typically treated with CSF shunting
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## References
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# Selected References
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1. [Adiyaman D et al: Contribution of fetal magnetic resonance imaging in the evaluation of neurosonographically detected cases of isolated mild and moderate cerebral ventriculomegaly. J Obstet Gynaecol Res. 48(9):2314-24, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=35778980%5Bpmid%5D)
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1. [D'Addario V: Diagnostic approach to fetal ventriculomegaly. J Perinat Med. ePub, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=36005554%5Bpmid%5D)
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1. [Bauer DF et al: Congress of Neurological Surgeons Systematic Review and Evidence-Based Guidelines on the Treatment of Pediatric Hydrocephalus: Update of the 2014 Guidelines. Neurosurgery. 87(6):1071-75, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=34791462%5Bpmid%5D)
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1. [Di Mascio D et al: Systematic review and meta-analysis on the role of prenatal magnetic resonance imaging in the era of fetal neurosonography: mild and moderate ventriculomegaly. Ultrasound Obstet Gynecol. 54(2):164-71, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30549340%5Bpmid%5D)
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1. [Katz JA et al: Utility of prenatal MRI in the evaluation and management of fetal ventriculomegaly. J Perinatol. 38(11):1444-52, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=30158676%5Bpmid%5D)
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1. [Orrù E et al: The child with macrocephaly: differential diagnosis and neuroimaging findings. AJR Am J Roentgenol. 210(4):848-59, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29470161%5Bpmid%5D)
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1. [Rashid QT et al: Time trends and age-related etiologies of pediatric hydrocephalus: results of a groupwise analysis in a clinical cohort. Childs Nerv Syst. 28(2):221-7, 2012](http://www.ncbi.nlm.nih.gov/pubmed/?term=21818584%5Bpmid%5D)
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1. [Kurihara Y et al: MR imaging of ventriculomegaly--a qualitative and quantitative comparison of communicating hydrocephalus, central atrophy, and normal studies. J Magn Reson Imaging. 5(4):451-6, 1995](http://www.ncbi.nlm.nih.gov/pubmed/?term=7549210%5Bpmid%5D)
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## Images
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### Selected Images
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**Fetal Ventriculomegaly**
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*Transverse oblique US in an 18-week fetus shows mild enlargement of the lateral ventricles <img src='img/arrows/CS.png'/> (11 mm). If the ventriculomegaly worsens later in pregnancy, fetal or postnatal MR imaging should be obtained.*
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**Fetal Ventriculomegaly**
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*Transverse oblique US in an 18-week fetus shows mild enlargement of the lateral ventricles <img src='img/arrows/CS.png'/> (11 mm). If the ventriculomegaly worsens later in pregnancy, fetal or postnatal MR imaging should be obtained.*
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**Fetal Ventriculomegaly**
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*Axial T2 SSFSE MR in a fetus shows marked enlargement (> 15 mm) of the lateral ventricles <img src='img/arrows/BS.png'/> & thinning of the cerebrum <img src='img/arrows/BC.png'/>. With severe fetal ventriculomegaly (particularly in the setting of aqueductal stenosis), the septum pellucidum (& even the cerebral mantle) may become disrupted.*
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**Benign Enlargement of Subarachnoid Spaces**
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*Coronal T2 MR in a 1-year-old with macrocephaly shows mild enlargement of the lateral <img src='img/arrows/CS.png'/> & 3rd <img src='img/arrows/CC.png'/> ventricles with moderate enlargement of the bifrontal subarachnoid spaces (SAS), which are traversed by normal veins <img src='img/arrows/CO.png'/>. Mild ventriculomegaly is often seen in benign enlargement of subarachnoid spaces (BESS).*
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**Benign Enlargement of Subarachnoid Spaces**
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*Coronal color Doppler US in a 9-month-old with BESS shows normal vessels <img src='img/arrows/CO.png'/> coursing through prominent fluid <img src='img/arrows/CS.png'/>, an expected finding that helps differentiate the SAS from subdural collections.*
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**Chiari 2 Malformation**
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*Sagittal 3D SSFP MR in a neonate with a myelomeningocele shows marked enlargement of the lateral ventricles <img src='img/arrows/BS.png'/> & characteristic features of Chiari 2 malformation: Small posterior fossa, brainstem & cerebellar descent <img src='img/arrows/CS.png'/>, tectal beaking <img src='img/arrows/CC.png'/>, & scalloped clivus <img src='img/arrows/CO.png'/>.*
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**Aqueductal Stenosis**
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*Sagittal T2 MR in a neonate shows massive enlargement of the lateral ventricles <img src='img/arrows/BS.png'/> due to obstruction at the level of the cerebral aqueduct <img src='img/arrows/CS.png'/>. The 3rd ventricle is also enlarged <img src='img/arrows/CO.png'/>, but the 4th ventricle is normal, typical of this disorder.*
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**Posthemorrhagic Hydrocephalus**
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*Sagittal T2 MR in a 1-month-old former premature infant with posthemorrhagic hydrocephalus shows marked enlargement of the lateral <img src='img/arrows/BS.png'/>, 3rd <img src='img/arrows/BO.png'/>, & 4th <img src='img/arrows/BC.png'/> ventricles. Note the dark hemosiderin lining the pial surface of the brainstem <img src='img/arrows/CS.png'/> from prior intraventricular hemorrhage (IVH).*
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**Posthemorrhagic Hydrocephalus**
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*Axial SWI MR in a 3-month-old former premature infant with posthemorrhagic hydrocephalus shows signal loss along the ependymal margins <img src='img/arrows/CS.png'/> of the ventricles & choroid plexus <img src='img/arrows/CO.png'/>, consistent with prior IVH.*
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**Acute Infectious Hydrocephalus**
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*Axial T1 C+ MR in a 7-year-old with Haemophilus influenzae meningitis shows marked expansion of the bifrontal SAS <img src='img/arrows/CS.png'/> & mild enlargement of the lateral ventricles <img src='img/arrows/CO.png'/>.*
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**Postinfectious Hydrocephalus**
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*Axial T1 C+ FS MR in an 8-month-old with tuberculous meningitis shows extensive basilar leptomeningeal enhancement <img src='img/arrows/CS.png'/> & enlargement of the lateral ventricles <img src='img/arrows/CO.png'/>, resulting in macrocephaly. Granulomatous infections are more likely to result in hydrocephalus compared to other bacterial meningitis.*
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**Obstructing Tumor**
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*Sagittal FLAIR MR in a neonate with a large, obstructing, hemorrhagic posterior fossa mass <img src='img/arrows/CO.png'/> shows enlargement of the lateral ventricles <img src='img/arrows/CS.png'/> & posterior fossa. Note the ↑ craniofacial ratio.*
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**CSF Overproduction (Choroid Plexus Tumor)**
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*Coronal T1 C+ MR in a 1-year-old with a choroid plexus papilloma shows an enhancing mass <img src='img/arrows/CS.png'/> in the right choroid plexus. The lateral ventricles are enlarged without evidence of obstruction. Hydrocephalus in this case is due to overproduction of CSF by the tumor.*
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**Hypoxic-Ischemic Injury**
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*Axial FLAIR MR in a 4-year-old with a history of perinatal hypoxic-ischemic injury (HII) shows extensive areas of cortical encephalomalacia <img src='img/arrows/CS.png'/>. Note the localized areas of ventriculomegaly <img src='img/arrows/CO.png'/> due to overlying brain volume loss.*
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**Hypoxic-Ischemic Injury**
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*Axial T2 MR in a 2-year-old with a history of perinatal HII shows symmetric areas of signal abnormality & volume loss involving the thalami <img src='img/arrows/CS.png'/>, putamina <img src='img/arrows/CO.png'/>, & periventricular white matter <img src='img/arrows/CC.png'/>, resulting in enlargement of the lateral <img src='img/arrows/BO.png'/> & 3rd <img src='img/arrows/BS.png'/> ventricles.*
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**Arterial Ischemic Stroke**
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*Axial T2 MR in a 9-month-old with previous infarction shows extensive cystic encephalomalacia <img src='img/arrows/CO.png'/> in right middle cerebral artery (MCA) territory with resultant asymmetric enlargement of the right lateral ventricle <img src='img/arrows/CS.png'/>.*
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**Periventricular Leukomalacia**
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*Axial FLAIR MR in a 7-year-old with a history of extreme prematurity & periventricular leukomalacia (PVL) shows symmetric focal enlargement of the atria <img src='img/arrows/CO.png'/> with adjacent white matter volume loss. The relative lack of abnormal FLAIR signal compared to the degree of volume loss is typical of PVL.*
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**Porencephaly**
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*Coronal US at 2 days of life in an extremely premature (23-week) infant shows a large right germinal matrix hemorrhage <img src='img/arrows/CS.png'/> with associated hemorrhagic venous infarction <img src='img/arrows/CO.png'/> in the right frontoparietal white matter.*
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**Porencephaly**
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*Coronal T2 MR in the same patient 3 months later shows the expected development of right parietal porencephaly & focal ventricular enlargement. Note the rim of T2 hypointensity <img src='img/arrows/CS.png'/>, related to hemosiderin, which will eventually resolve.*
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**Metabolic Brain Disease**
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*Axial T2 MR in a teenager with metachromatic leukodystrophy shows ↑ signal & volume loss in the periventricular & deep white matter <img src='img/arrows/CS.png'/> with sparing of the subcortical white matter, characteristic of this disease. Note the enlargement of the lateral ventricles <img src='img/arrows/CO.png'/> & sulci <img src='img/arrows/CC.png'/> due to the brain volume loss.*
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**Metabolic Brain Disease**
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*Axial T2 MR in a teenager with vanishing white matter disease shows extensive ↑ signal intensity & volume loss in the white matter <img src='img/arrows/CS.png'/> with associated enlargement of the lateral <img src='img/arrows/BS.png'/> & 3rd <img src='img/arrows/BO.png'/> ventricles & sulci <img src='img/arrows/CO.png'/>.*
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**Hemimegalencephaly**
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*Axial T1 MR in a neonate with seizures & hemimegalencephaly shows ↑ size of the left parietooccipital hemisphere with loss of normal sulcation <img src='img/arrows/CS.png'/> & markedly abnormal neuronal organization <img src='img/arrows/CO.png'/>. Also note enlargement of the ipsilateral occipital horn <img src='img/arrows/CC.png'/>.*
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**Hemimegalencephaly**
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*Axial T1 MR in a 3-day-old with left hemimegalencephaly shows marked occipital horn enlargement <img src='img/arrows/CO.png'/>. Note the abnormal white matter <img src='img/arrows/CS.png'/> in the left frontal lobe. Enlargement of the ipsilateral occipital horn is common in this disease.*
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**Vein of Galen Aneurysmal Malformation**
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*Coronal T2 MR in a neonate with VGAM shows a markedly enlarged central vein <img src='img/arrows/CO.png'/> with numerous enlarged choroidal <img src='img/arrows/CC.png'/> & pericallosal <img src='img/arrows/CS.png'/> feeding arteries. Note the enlarged ventricles <img src='img/arrows/BS.png'/>, which are likely due to ↓ resorption of CSF due to ↑ venous pressures.*
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**Dandy-Walker Malformation**
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*Sagittal 3D SSFP MR in a 2-month-old with Dandy-Walker malformation shows a small cerebellar vermis <img src='img/arrows/CO.png'/> & large posterior fossa cyst <img src='img/arrows/CS.png'/> that is continuous with the 4th ventricle. There is elevation of the tentorium & torcular Herophili <img src='img/arrows/CC.png'/>.*
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**Hydranencephaly**
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*Axial NECT in a 4-year-old with hydranencephaly shows porencephaly in the bilateral MCA <img src='img/arrows/CO.png'/> & left anterior cerebral artery (ACA) <img src='img/arrows/CS.png'/> territories in continuity with the lateral ventricles. Note the intact falx <img src='img/arrows/CC.png'/>. Patients with hydranencephaly typically become macrocephalic due to poor CSF regulation.*
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**Holoprosencephaly**
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*Sagittal T2 MR in a neonate with holoprosencephaly shows an enlarged monoventricle <img src='img/arrows/CS.png'/>. However, the patient is microcephalic overall due to the ↓ brain parenchymal volume.*
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